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  • Author or Editor: Stephen M. Boyle x
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SUMMARY

Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoileal morphology were examined in neonatal calves infected with Cryptosporidium parvum. Group-1 calves served as noninfected controls and, after an adjustment period, were given 50 ml of saline solution iv every 12 hours for 6 days. Group-2 calves were inoculated with 107 C parvum oocysts and, after the onset of diarrhea, were given 50 ml of saline solution iv every 12 hours for 6 days. Group-3 calves were inoculated with 107 C parvum oocysts and, after the onset of diarrhea, were treated with difluoromethylornithine (dfmo, 200 mg/kg of body weight iv, q 12 h) for 6 days. Group-4 calves were naturally infected with C parvum. Jejunoileal biopsy specimens were excised from calves of groups 1-3 at 3 and again at 15 to 16 days of age. During the course of diarrhea and 3 days after saline or dfmo administration, water-miscible retinyl palmitate was administered orally (2,750 μg/kg) to each calf in each group. Cryptosporidium parvum infection was associated with significant (P ≤ 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, and 4. Cryptosporidium parvum infection caused significant (P ≤ 0.05) reduction in villus height. Decreased villus height, villus blunting and fusion, and attenuation of the intestinal mucosa were associated with reduced absorption of vitamin A, as indicated by lower peak postadministration retinyl palmitate concentration in C parvum-infected calves. Intravenous administration of dfmo to group-3 calves did not improve retinol absorption. Vitamin A should be provided parenterally to young calves with enteric cryptosporidiosis in an attempt to avoid depletion of concurrent low liver vitamin A reserves.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To evaluate stable rough mutants derived from Brucella melitensis 16M and B suis 2579 (biovar 4) as vaccines against homologous and heterologous Brucella spp in the BALB/c mouse model.

Design, Animals, and Procedure

Rough mutants VTRM1 and VTRS1 were obtained from B melitensis 16M and B suis 2579, respectively, by allelic exchange of the rfbU gene encoding mannosyltransferase with a Tn5-disrupted rfbU gene. Mice were vaccinated with VTRM1 or VTRS1 and challenge exposed 8 weeks later.

Results

VTRM1 and VTRS1 replicated extensively in the spleen during the first 3 weeks of infection, then decreased rapidly. Antibodies specific for the O polysaccharide were not detected in sera of mice inoculated with either rough strain. Vaccination with VTRM1 or VTRS1 induced protection against virulent strains of B abortus (2308), B melitensis (16M), B suis biovar 1 (750), and B suis biovar 4 (2579). VTRM1 also protected against B ovis (PA) and against 4 field isolates of B abortus from bison or elk. VTRS1 conferred protection against 4 field isolates of B suis biovar 4 from reindeer. Vaccines prepared from live VTRM1 or VTRS1 provided significantly greater protection than that afforded by vaccines of killed cells in QS- 21 adjuvant. Vaccination with VTRM1 containing VTRS1 gave minimal protection against the antigenically unrelated Listeria monocytogenes, thus demonstrating the immunologic specificity of protection against Brucella spp.

Conclusions and Clinical Relevance

Results encourage evaluation, in primary host species, of VTRM1 and VTRS1, along with RB51, as alternative vaccines to strain 19, Rev 1, or other smooth phase vaccines. (Am J Vet Res 1996; 57:677–683)

Free access
in American Journal of Veterinary Research
Full access
in Journal of the American Veterinary Medical Association